The effect of Helicobacter pylori infection on apoptosis and cell proliferation in gastric epithelium.

Background/Aims: Helicobacter pylori (Hp) may affect the normal balance between gastric epithelial cell proliferation and epithelial cell death, interfering thus with the maintenance of gastric mucosa integrity. The aim of this study was to investigate the effect of Hp infection on cell proliferation index (PI) and apoptotic index (AI) in gastric epithelium of the antrum and corpus. Methodology: Prospective study in forty-one patients with functional dyspepsia (14 males, 27 females, average age = 54±16.1 years). Day one: upper digestive endoscopy with biopsies of the antrum and corpus, and a cytological smear of the antral area for AgNOR (argyrophilic nucleolar organizer region) analysis. Biopsies for the programmed tests were sent in separate labeled containers: to study AI (antibody anti-, PI (antibody anti-Ki 67) and histology (Sydney criteria and the detection of Hp). Detection of the AgNORs through the Gimenez-Mas et al. technique, using Visilog-Microptic Software. Day two: a blood sample was drawn from each patient for the serologic detection of the status CagA and VacA, and a breath test was carried out with 13 C-Urea. Statistics: SPSS program with the application of Student's t, chi-square and Fisher tests. Results: 24 patients were Hp(+) and 17 Hp(-). The PI (Ki 67 and AgNORs) in the antral area was significantly increased in the Hp(+) patients. AI showed no significant difference in the subgroups Hp(+) and Hp(-). Both subgroups showed increased PI in the antrum and increased AI in the gastric corpus. There was significantly higher PI in CagA(+), without an increase in the AI. The AI was significantly higher in CagA(-), when compared with CagA(+). The VacA protein had no influence on PI and AI. Acute and chronic gastritis was more frequent and more severe in Hp(+) patients. This group lacked any correlation between the histological findings and the PI, but the opposite was the case between AI and the degree of cellular infiltration. Conclusions: In patients with functional dyspepsia, Hp inflection induces an increase of PI, with significant presence in the antrum area, without the corresponding increase m AI. Cag A(+) promotes the increase of PI, and Cag A(-) promotes the increase of AI. The Vac A status has no influence on the PI or AI. The degree of cellular infiltration interferes with AI.